- RAS p21 protein activator 1
RAS p21 protein activator 1 or RasGAP (Ras GTPase activating protein), also known as RASA1, is a 120-
kDa cytosolic human protein that provides two principal activities:
* Inactivation ofRas from its active GTP-bound form to its unactive GDP-bound form by enhancing the endogenousGTPase activity of Ras, via its C-terminal GAP domain
* Mitogenic signal transmission towards downstream interacting partners through its N-terminal SH2-SH3-SH2 domainsPBB_Summary
section_title =
summary_text = The protein encoded by this gene is located in the cytoplasm and is part of the GAP1 family of GTPase-activating proteins. The gene product stimulates the GTPase activity of normal RAS p21 but not its oncogenic counterpart. Acting as a suppressor of RAS function, the protein enhances the weak intrinsic GTPase activity of RAS proteins resulting in the inactive GDP-bound form of RAS, thereby allowing control of cellular proliferation and differentiation. Mutations leading to changes in the binding sites of either protein are associated with basal cell carcinomas. Alternative splicing results in two isoforms where the shorter isoform, lacking the N-terminal hydrophobic region but retaining the same activity, appears to be abundantly expressed in placental but not adult tissues. [cite web | title = Entrez Gene: RASA1 RAS p21 protein activator (GTPase activating protein) 1| url = http://www.ncbi.nlm.nih.gov/sites/entrez?Db=gene&Cmd=ShowDetailView&TermToSearch=5921| accessdate = ]Domains
RasGAP contains one
SH3 domain and twoSH2 domain s, aPH domain , and aGAP domain .References
Further reading
PBB_Further_reading
citations =
*cite journal | author=Tocque B, Delumeau I, Parker F, "et al." |title=Ras-GTPase activating protein (GAP): a putative effector for Ras. |journal=Cell. Signal. |volume=9 |issue= 2 |pages= 153–8 |year= 1997 |pmid= 9113414 |doi=
*cite journal | author=Boon LM, Mulliken JB, Vikkula M |title=RASA1: variable phenotype with capillary and arteriovenous malformations. |journal=Curr. Opin. Genet. Dev. |volume=15 |issue= 3 |pages= 265–9 |year= 2005 |pmid= 15917201 |doi= 10.1016/j.gde.2005.03.004PBB_Controls
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